I have skeptical confession to make. I was once a panacea-seeking antioxidant-taker. As background, I’m a marathon runner and occasional triathlete. Several years ago, I was training for an Ironman triathlon, and banking 20+ hours of intense exercise per week. That may sound absurd to many (it does to me, now that I have kids) but that kind of training is necessary for the long races. So what did this pharmacist-wannabe-triathlete with access to discount vitamins do? He stocked up on the fancy bottles of multivitamins, the “endurance” version, of course — with extra antioxidants. Why did I supplement? I wanted to maximize my workouts, speed recovery, and minimize downtime and the risk of injury. Oxidation sounds bad — like a rusting car. Anti-oxidants sounded like the ultimate in preventative medicine. My workouts may have been more extreme, but the practice of supplementing if you exercise is common among athletes.
As it turns out, not only were the antioxidants likely ineffective, they may have compromised some of the gains I was seeking with all that training. That I didn’t evaluate the evidence at the time was my critical-thinking blind spot. Over the the past several years, more data on antioxidants and exercise have emerged. A recent review article, Read more »
*This blog post was originally published at Skeptic North*
Science has found no evidence that vaccines cause autism; but the true cause(s) of autism have not yet been determined. So far the available evidence has pointed towards a largely genetic cause with possible interaction with environmental factors. A new study supports that interpretation. It also supports previous evidence that autism is triggered prior to birth, rather than at the time of vaccinations.
Schmidt et al. published a study in Epidemiology on May 23, 2011, entitled “Prenatal Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism.” It was a population-based case control study of 566 subjects comparing a group of autistic children to a matched control group of children with normal development. They looked at maternal intake of prenatal vitamins in the 3 months before conception and the first month of pregnancy, and they looked for genotypes associated with autism. They found that mothers who didn’t take prenatal vitamins were at greater risk of having an autistic child, and certain genetic markers markedly increased the risk. There was a dose/response relationship: the more prenatal vitamins a woman took, the less likely she would have an autistic child. There was no association with other types of multivitamins, and no association with prenatal vitamin intake during months 2-9 of pregnancy.
They had a large sample size, and they tried to eliminate confounders. They looked for these potential confounders of the association between prenatal vitamin intake and autism: child’s sex, birth year, parent-reported race/ethnicity, family history of mental health conditions, paternal age at child’s birth, maternal age at child’s birth, education, prepregnancy body mass index (BMI) category, cereal intake from 3 months before through the first month of pregnancy, cigarette smoking, alcohol consumption, and residence with a smoker during the period 3 months before pregnancy to delivery. Only maternal education and the child’s year of birth proved to be confounders. They adjusted for these two factors in their analyses. A weakness of their study is that it depends on patient recall long after the fact. Also, it did not attempt to gather any diet information.
Mothers of children with autism were less likely to report taking prenatal vitamins (odds ratio 0.62). Having certain genotypes increased the odds that a vitamin-omitting woman would have an autistic child. Children with the COMT 472 AA gene were at increased risk of autism. If their mothers took prenatal vitamins, the odds ratio for the risk of autism was 1.8; if their mothers didn’t, the odds ratio jumped to 7.2. This suggests that the maternal-fetal environment can magnify the effects of a child susceptibility gene. There was an association with certain maternal genes as well: those odds ratios went as high as 4.5.
The association was robust. The authors think Read more »
*This blog post was originally published at Science-Based Medicine*